关键词: aerobic exercise training myocardium proteomics rat supravalvular aortic stenosis ventricular dysfunction

Mesh : Animals Rats Aortic Valve Stenosis / metabolism Inflammation Lipids Physical Conditioning, Animal / methods Proteome Proteomics Rats, Wistar Myocardium / metabolism

来  源:   DOI:10.1002/jcp.31199

Abstract:
The effects of exercise training (ET) on the heart of aortic stenosis (AS) rats are controversial and the mechanisms involved in alterations induced by ET have been poorly clarified. In this study, we analyzed the myocardial proteome to identify proteins modulated by moderate-intensity aerobic ET in rats with chronic supravalvular AS. Wistar rats were divided into four groups: sedentary control (C-Sed), exercised control (C-Ex), sedentary aortic stenosis (AS-Sed), and exercised AS (AS-Ex). ET consisted of five treadmill running sessions per week for 16 weeks. Statistical analysis was performed by ANOVA or Kruskal-Wallis and Goodman tests. Results were discussed at a significance level of 5%. At the end of the experiment, AS-Ex rats had higher functional capacity, lower blood lactate concentration, and better cardiac structural and left ventricular (LV) functional parameters than the AS-Sed. Myocardial proteome analysis showed that AS-Sed had higher relative protein abundance related to the glycolytic pathway, oxidative stress, and inflammation, and lower relative protein abundance related to beta-oxidation than C-Sed. AS-Ex had higher abundance of one protein related to mitochondrial biogenesis and lower relative protein abundance associated with oxidative stress and inflammation than AS-Sed. Proteomic data were validated for proteins related to lipid and glycolytic metabolism. Chronic pressure overload changes the abundance of myocardial proteins that are mainly involved in lipid and glycolytic energy metabolism in rats. Moderate-intensity aerobic training attenuates changes in proteins related to oxidative stress and inflammation and increases the COX4I1 protein, related to mitochondrial biogenesis. Protein changes are combined with improved functional capacity, cardiac remodeling, and LV function in AS rats.
摘要:
运动训练(ET)对主动脉瓣狭窄(AS)大鼠心脏的影响存在争议,而ET引起的改变的机制尚不清楚。在这项研究中,我们分析了心肌蛋白质组,以鉴定中度强度有氧ET在慢性瓣膜上AS大鼠中调节的蛋白质。Wistar大鼠分为四组:久坐对照(C-Sed),行使控制权(C-Ex),久坐的主动脉瓣狭窄(AS-Sed),并作为(AS-Ex)行使。ET包括每周五次跑步机跑步,持续16周。通过ANOVA或Kruskal-Wallis和Goodman检验进行统计分析。在5%的显著性水平下讨论结果。实验结束时,AS-Ex大鼠具有较高的功能能力,降低血乳酸浓度,心脏结构和左心室(LV)功能参数优于AS-Sed。心肌蛋白质组分析表明,AS-Sed具有较高的糖酵解途径相关蛋白丰度,氧化应激,和炎症,与β-氧化相关的相对蛋白质丰度低于C-Sed。与AS-Sed相比,AS-Ex的一种与线粒体生物发生相关的蛋白质丰度更高,而与氧化应激和炎症相关的相对蛋白质丰度更低。对与脂质和糖酵解代谢相关的蛋白质的蛋白质组数据进行了验证。慢性压力超负荷改变了主要参与大鼠脂质和糖酵解能量代谢的心肌蛋白的丰度。中等强度有氧训练减弱与氧化应激和炎症相关的蛋白质的变化,并增加COX4I1蛋白,与线粒体生物发生有关。蛋白质的变化与功能能力的提高相结合,心脏重塑,和AS大鼠的LV功能。
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